DOMS Treatments (long but good)
- 06-11-2003, 09:17 AM
DOMS Treatments (long but good)
Exercise Physiology 652 (1998) Debate:
There is a role for physiotherapy in ameliorationg the DOMS response to EIMD!
by Mia Creagh and Beate Lokken
Affirmative Argument by Mia Creagh
Background / New Knowledge:
Delayed Onset Muscle Soreness (DOMS) is pain or discomfort in muscles that have undergone unaccustomed exercise. Eccentric exercise produces greater soreness, fatigue and damage than isometric and concentric contractions (Clarkson and Newham 1995). It is a temporary condition characterised by time course of pain following activity. The soreness usually develops within 24 hours of exercise and is characterised by a dull ache with tenderness and stiffness. Soreness subsides within 5 to 7 days regardless of further activity (Stauber 1996).
Various authors have proposed different mechanisms of injury following eccentric exercise, however very little is known about the mechanisms involved in the production of DOMS or the accompanying responses such as prolonged loss of ROM and strength, increased muscle enzymes in the blood, swelling and structural damage (Clarkson and Newham 1995). It is thought that firstly a mechanical injury followed by a biochemical injury is responsible for the changes in the muscle following eccentric exercise (MacIntyre et al 1995).
Histological and ultrastructural changes range from mild damage where single sarcomeres throughout the muscle show evidence of Z line streaming or bulging with extension into the A band and myofibrillar disruption. More severe damage results in cytoskeletal and myofibrillar damage, oedema, invading mononuclear cells, muscle fibre atrophy and necrosis. Regeneration occurs from 10 days for mild damage up to three weeks for severe damage (Clarkson and Newham 1995). Increased tension per individual cross-bridge causes mechanical disruption of the ultrastructural elements within muscle fibres such as the Z line (Z line streaming) and contractile filaments. Changes in the Z-line are attributed to loss of alpha-actin and vimentin (MacIntyre et al 1995).
Stauber et al (1996) suggests that a complex set of reactions including disruption of muscle fibre and connective tissue (CT) is responsible for DOMS. CT damage involves endomysial separations which is assumed to occur during exercise. The injury may result from cytoskeletal damage to the intermediate filaments (desmin, Vimentin and synemin) or proteolytic enzymes may be released from the initial injury causing further degradation of the cytoskeleton (MacIntyre et al 1995).
Progressive structural damage (Metabolic Injury?):
Mechanisms proposed for the progressive nature of structural damage include accumulation of intracellular calcium following the mechanical insult. This triggers calcium mediated processes. It appears that fast twitch fibres are most affected as they fatigue early and enter a high state of stiffness due to an inability to regenerate ATP. Subsequent stretch mechanically disrupts the fibres causing cytoskeletal and myofibrillar damage (Clarkson and Newham 1995).
Sarcolemma damage leads to disruption of muscle cell calcium homeostasis resulting in increased intracellular calcium concentration. This results in further muscle contractile protein and membrane degeneration which is likely to be caused by calcium induced activation of muscle protease and phospholipidase enzymes. Markers of muscle damage and membrane disruption such as CK are evident in the blood at this time. These factors are proposed to cause prolonged reductions in muscular strength (Tiidus 1997).
Following skeletal muscle damage several intramuscular proteins leak into the blood including creatine kinase (CK), myoglobin, lactate dehydrogenase, aspartate aminotransferase, myosin heavy chain fragments. These are elevated following eccentric exercise. There is a delay in the appearance of these proteins in the blood from24-72 hours. It is suggested that the release and slow removal from extracellular spaces provide colloid osmotic pressure to produce oedema (Clarkson and Newham 1995).
To date the role of inflammation during exercise induced muscle injury has not been clearly defined. The role of neutrophil infiltration in exercise-induced muscle injury is not known although several studies have reported that macrophages were the predominant inflammatory cell present in exercise induced muscle injury. Different subpopulations of macrophages have been associated with distinct stages of recovery following muscle injury (Smith 1991).
Smith (1991) suggests the sequence of events with DOMS begins with connective and contractile tissue injury. A significant elevation in circulating neutrophils follows at approximately 3 hours and migration to the site of injury. Monocytes then emigrate at 6-12 hours with large numbers present at 24 hours peaking at 48 hours. The macrophages synthesise PGE2 which sensitises type III and IV pain afferents. Bradykinin, histamine, serotonin and achetylcholine also sensitise pain afferents (Smith 1991).
The Cause of Muscle Soreness:
The exact cause is unknown however inflammation and swelling are considered prime factors (Smith 1991). Fluid accumulates in the muscle for five days after exercise then moves into the subcutaneous area as demonstrated in MRI studies. Swelling within the muscle compartment could produce pain and increase intramuscular pressure in low compliance compartments. It may also result in sensitisation of pain receptors to other noxious stimuli (Clarkson and Newham 1995).
Slow release of cellular infiltrates from damaged cells may explain the delayed sensation of soreness associated with an acute inflammatory response (Clarkson and Newham 1995). The reason soreness is present on movement or palpation but not at rest is that the former increases intramuscular pressure and stimulate sensitised pain receptors (Smith 1991).
Loss of muscle function:
This has been observed up to one hour following exercise. It may take up to two weeks for maximal recovery of isometric strength. It has been demonstrated that little or no relationship exists between the development of soreness and the loss of muscle strength. Therefore reduced performance occurs due to muscle tissue damage independant of pain induced inhibition of muscle (Clarkson and Newham 1995). It is not clear whether the initial loss in muscle strength is due to muscle injury, fatigue or both. It is proposed that immediate strength reduction is due to overstretched sarcomeres with reduced overlap between actin and myosin. Some sarcomeres may maintain their length and others are overstretched beyond overlap. This relates to findings of greater strength deficits at long compared to short muscle lengths (MacIntyre et al 1995).
Two declines in muscle strength have been reported following eccentric exercise. The greatest decline in eccentric torque immediately follows exercise then partially recovers (2-4 hrs) and declines again 20-24 hours post exercise. It is suggected that a secondary biochemical injury results in free radical production by injured tissue from the phagocytic activity at the site of the original damage. Neutrophils and macrophages release oxygen radicals and proteases with the potential to cause further damage (MacIntyre et al 1995; Stauber et al 1996).
The Cause of Stiffness:
Stiffness following eccentric activity is suggested to be the result of swelling and spontaneous shortening due to the abnormal accumulation of calcium inside the muscle cell as a result of loss of sarcolemma integrity or dysfunction of the sarcoplasmic reticulum (Clarkson and Newham 1995). The immediate increase in stiffness is thought to be the result of altered calcium homeostasis. Stiffness is then influenced by swelling which peaks on day 4. Stiffness declines by day 7-11 in accordance with reduction in swelling (Chleboun et al 1998).
1) The Preventative Effect of Training:
It is believed that training prevents or reduces muscle damage and consequent soreness. DOMS only occurs following the first or second bouts of a new exercise program. Studies assessing CK activity (which indirectly assesses muscle damage) following a training program report reduced serum CK in response to a given exercise. Suggestions for this phenomenon initially centred around damage to a pool of fragile or stress susceptible muscle fibres resulting in a large serum CK response. The dynamic process of degeneration-regeneration that follows results in fewer stress susceptible muscle fibres on repetition of the exercise. More recent evidence has suggested that training does not eliminate a stress susceptible fibre population but provides a sufficient stimulus to increase the resistance of muscle fibres to injury (Armstrong 1990, Byrnes et al 1986).
Friden et al (1983) demonstrated that the negative effects of eccentric exercise could be reduced by eccentric training. 15 subjects cycled 2-3 times per week for 4-8 weeks on a bicycle ergometer modified for use in eccentric work. Each time they cycled until severe fatigue at progressively increased work intensities. All subjects suffered from pronounced soreness of the knee extensors after the first 3-4 stints but following this symptoms gradually decreased and all subjects were free from complaints following 2-3 weeks of training. Additionally, following the eight weeks of training a single episode of maximal eccentric work caused a negligible decrease in maximal dynamic strength and a dramatic improvement in maximal eccentric work capacity was noted. Following the eight week training period, type 2B fibers were preferentially recruited. This coordination effect was proposed to lead to fewer units being recruited (Friden et al 1983). The protective effect of endurance training may convert type 2B to type 2A fibres thereby preventing type 2B fibre fatigue with eccentric exercise (Friden and Lieber 1992).
Stauber (1991) recommends prevention of DOMS by emphasising types of exercises producing less damage early in any training or rehabilitation program. He suggests a program using specific muscles in shortened positions under mild loads then gradually increasing ROM with each training session until the muscle is active throughout the entire range. The best prevention is regular exercise and repetition of an activity containing eccentric muscle activity to protect the muscle from repeated injury.
2) Effects of Compression:
The relationship between swelling and stiffness was highlighted in a study by Chleboun et al (1995) in which external pneumatic compression was applied daily for five days to the arm following exercise induced muscle injury. A reduction in arm circumference and stiffness on days two and three post exercise was demonstrated, although strength loss was not affected (Chleboun et al 1995).
3) Effects of Cryotherapy:
Very few studies have investigated the effects of cryotherapy on muscle soreness and strength following eccentric exercise. Of those that have addressed this issue the results suggest there are limited benefits. However, the methodology of these experiments is questionable in light of the characteristics of muscle oedema highlighted by Chleboun et al (1998).
Paddon-Jones and Quigley (1997) found no significant difference between the immersed and control arms in recovery of elbow flexor strength and reducing the severity of DOMS following eccentric exercise. They suggest there is no therapeutic benefits of cryotherapy immediately following damaging eccentric exercise. However, the sample size of eight was very small to make these conclusions. The protocol of cryotherapy employed consisted of 5x20 minute immersions in ice water which commenced immediately following exercise with 60 minute rest periods between applications. The time of application may be inappropriate in light of recent evidence that swelling increase to peak on day 4! (Chlebourn et al 1998). It is possible that a greater number of cold applications would be required to significantly influence recovery. The method of measurement of arm volume was not specific to the compartments affected by the eccentric exercise. The protocol involved immersion, collection and weighing of water overflow. Possibly an ultrasonic method similar to that employed in the Chlebourn et al (1998) study would have been more specific.
4) Effects of Massage:
There is limited research substantiating the routine use of sports massage in speeding recovery from vigorous exercise. Most studies concluding massage as ineffective have administered it either immediately after exercise or 24-48 hours following exercise (Smith et al 1994).
Smith et al (1994) investigated the effects of athletic massage on DOMS, creatine kinase (CK) and neutrophil count in fourteen untrained subjects following eccentric isokinetic contractions of the biceps. Two hours following the exercise bout a thirty minute sports massage or a placebo was performed. The massage involved effleurage and petrissage. The choice of the two hour post exercise administration of massage was based on the principles of restorative massage used by the Soviet sports therapists at the time, which was reported to enhance relaxation and restoration of the athletes body. It is proposed that masssage between 1-3 hours post exercise interferes with the initiation of the acute inflammatory response. The critical event during this time is the accumulation of neutrophils followed by a decline in their circulation as they marginate to the vessel walls and subsequently emigrate to the traumatised tissue. The subsequent accumulation of macrophages depends on the initial accumulation of neutrophils. This process has been reported following eccentric exercise. It is hypothesised that massage disrupts margination and subsequent emigration of neutrophils into the area of injury causing prolonged elevation of circulating neutrophils thereby reducing the intensity of inflammation and reducing pain and discomfort associated with DOMS. Results indicated significantly reduced levels of DOMS and CK, prolonged elevation of neutrophils and diminished diurnal reduction in cortisol in the massaged group. The rationale behind massage causing these effects is based on the premis that massage increases blood flow through the vascular beds preventing margination of neutrophils. The vigorous nature of the massage would additionally shear marginated cells from vessel walls and hinder emigration of cells from the circulation into tissue spaces. The lower CK levels in the massaged group may be due to CK efflux as a result of mobilisation of neutrophils at the site of injury. During the eight hour post exercise period the massaged group showed less reduction in cortisol levels possibly due to the body interpreting the vigorous massage as stress thereby increasing the release of cortisol into the circulation. Glucocorticoids have profound anti-inflammatory properties. They inhibit neutrophil adherence to vessel walls interfering with emigration.
Application of a second sensation such as massage to a sore muscle could increase discharge from other low threshold sensory fibres thereby temporarily blocking the sensation of soreness. It is suggested that light exercise also temporarily diminishes muscle soreness by this mechanism. If oedema, swelling and inflammation are significant factors in the sensation of muscle soreness then massage may reduce their presence and affect soreness (Tiidus 1997).
Studies investigating the effect of massage on skeletal blood flow have produced conflicting results. The differences may be accounted for by the different sizes of muscles studied and the type of massage employed. Smaller muscles report increased blood flow although a larger muscle mass may reduce the ability of topical pressures to induce emptying of deeper capillaries (Tiidus and Shoemaker 1995). Tiidus and Shoemaker (1995) found a small but significant tendency for massage to reduce DOMS after 48 hours post exercise and propose that massage induces an analgesic effect on muscle sensory receptors and induces physiological relaxation.
5) Effects of Light Exercise:
Light muscle contractions have been found to improve blood flow in muscle even more effectively than manual massage as shown on Dopper ultrasound. If enhanced muscle blood flow improves healing then light muscle contractions should be more effective than massage (Tiidus 1997).
Performing light exercise with exercise damaged muscles is reported to temporarily reduce soreness (Tiidus 1997). Continuing light exercise immediately following intense activity enhances muscle blood flow and thereby improves oxygen and nutrient delivery. This will aid recovery from muscle fatigue by enhancing the efflux of lactate and hydrogen ions from muscle. Elevation of hydrogen ions is caused by decreased muscle potassium, increased phosphocreatine breakdown and increased muscle carbon dioxide levels. The hydrogen interferes with the ability of muscle contractile proteins to generate force by reducing the total number of cross bridges formed or the force generated per cross bridge. Therefore simple warm-down exercises would enhance short term recovery (Tiidus 1997).
Tiidus and Shoemaker (1995) report significantly elevated arterial and venous blood velocity above resting levels in the quadriceps muscle following light quadriceps muscle contractions.
Hasson et al (1989) found a therapeutic regimen of high speed voluntary muscle contractions following eccentric exercise was effective in decreasing muscle soreness and facilitating return of normal muscular performance. Maximal voluntary contraction, peak torque and total work of the quads showed a significant reduction in percent decrease from baseline. Soreness perception index was significantly less at 48 hours post muscle soreness. The regimen consisted of 20 voluntary maximal knee extension and flexion contractions at 300 degrees per second with 3 minutes recovery repeated for 6 sets. This was initiated 24 hours post exercise. The authors suggest that concentric muscle contractions especially at submaximal levels do not produce tissue damage and therefore do not elicit an inflammatory response. Additionally, the "muscle pump action" reduces oedema and intramuscular pressure.
6) Effects of Ultrasound:
Hasson et al (1990) found soreness perception following pulsed ultrasound was significantly less at 48 hours post exercise compared to a placebo and control. Muscle performance also significantly improved in the ultrasound group however values remained significantly lower than baseline values. 18 subjects were tested with the ultrasound group receiving 0.8 w/cm2 pulsed ultrasound (1:4 ratio). This treatment intensity has been shown to elicit anti-inflammatory effects and fluid streaming in the tissue. Streaming may alter vascular permeability and lessen the pressure gradient across the myosium. The dose was administered 24 hours post exercise however the authors suggest that immediate delivery of ultrasound to control the initial inflammation and reduce muscle oedema and intracompartmental pressures may improve results.
Hasson et al (1992) investigated the effects of dexamethasone iontophoresis on DOMS. Iontophoresis consisted of direct current for 20 minutes at varying intensities. DOMS was significantly slowed from 24 to 48 hours compared to the placebo and control groups. There was no significant difference in muscle function indicating that soreness perception and muscle function are not directly related. Iontophoresis has become a method of drug administration for therapists as it permits constant drug delivery over a specific amount of time and provides a highly localised drug concentration and low systemic dose of the drug. The anti-inflammatory action of dexamethasone occurs when the corticosteroid combines to cellular membrane sites and inhibits prostaglandin formation and secretion.
The exact cause of the pain in DOMS is not known although clinicians acknowledge damage to skeletal muscle via exercise as responsible for the perception of pain. As the condition is self limiting, medical attention is seldom required (MacIntyre et al 1995).
Clinical examination reveals restricted range of motion, localised muscle tenderness and weakness. There is no pain at rest but discomfort with any movement developing muscle tension (MacIntyre et al 1995).
Prevention should be emphasised through regular exercise, endurance training and repetition of eccentric activity. The intrinsic process of adaptation with eccentric exercise training reduces muscle damage and soreness. Stauber (1996) suggests emphasis should be placed on exercise producing less damage early in a training regimen. Initially muscles may be used in shortened positions with mild loads, gradually progressing the load and increasing the range of movement until the muscle is active throughout the entire range.
One of the most effective means of reducing DOMS is via active-resisted exercise of the affected muscle groups. Submaximal exercise enhances short term recovery by increasing blood flow.
To enhance recovery a variety of treatments may be utilised. Intermittent pneumatic compression has been shown to reduce swelling and stiffness especially on days 2-3 post exercise. Cryotherapy requires further investigation to substantiate its use following EIMI. Research needs to be conducted investigating the effect of ice in isolation and for a longer time frame into the period of peak swelling on day 4. Massage may be effective if performed 2 hours following exercise to increase blood flow and disrupt the inflammatory reaction. Additionally there is an analgesic effect on sensory receptors and physiological relaxation is induced. Ultrasound within 24 hours improves muscle performance and reduces DOMS. The parameters demonstrated to be most effective are 0.8 W/cm2 with a 1:4 ratio on pulsed producing anti-inflammatory effects and fluid streaming. Finally, iontophoresis is a useful adjunct to treatment.
Armstrong RB (1990): Initial events in exercise-induced muscular injury. Medicine and Science in Sports and Exercise 22:429-435.
Byrnes WC, Priscilla FR and Clarkson PM (1986): Delayed onset muscle soreness and training. Clinics in Sports Medicine 5:605-614.
Chleboun GS, Howell JN, Conaster RR and Giesey JJ (1998): Relationship between muscle swelling and stiffness after eccentric exercise. Medicine and Science in Sports and Exercise 30:529-535.
Chleboun GS, Howell JN, Heather LB, Ballard TN, Graham JL, Hallman HL, Perkins LE, Schauss JH and Conatser RR (1995): Intermittent pneumatic compression effect on eccentric exercise-induced swelling, stiffness and strength loss. Archives of Physical Medicine and Rehabilitation 76:744-749.
Clarkson PM and Newham DJ (1995): Associations between muscle soreness, damage, and fatigue. In Gandevia SC, Enoka RM, McComas AJ Stuart DG and Thomas CK (Eds): Fatigue: Neural and muscular mechanisms.New York:Plenum Press pp457-469.
Friden J and Lieber RL (1992): Structural and mechanical basis of exercise-induced muscle injury.Medicine and Science in Sports and Exercise 24:521-530.
Friden J, Seger J, Sjostrom M, and Ekblom B (1983): Adaptive response in human skeletal muscle subjected to prolonged eccentric training. International Journal of Sports Medicine 4:177-183.
Hasson S, Barnes W, Hunter M and Williams J (1989): Therapeutic effect of high speed voluntary muscle contractions on muscle soreness and muscle performance. Journal of Orthopaedic and Sports Physical Therapy 10:499-504.
Hasson SM, Wible CL, Barnes WS, and Williams JH (1992): Dexamethasone iontophoresis: Effect on delayed muscle soreness and muscle function. Canadian Journal of Sport Sciences 17:8-13
Hasson S, Munorf R, Barnes W Williams J and Fujii M (1990): Effect of pulsed ultrasound versus placebo on muscle soreness perception and muscular performance. Scandinavian Journal of Rehabilitation Medicine 22:199-205.
MacIntyre DL, Reid WD and McKenzie DC (1995): Delayed muscle soreness. Sports Medicine 20:24-40.
Paddon-Jones DJ and Quigley BM (1997): Effect of cryotherapy on muscle soreness and strength following eccentric exercise. International Journal of Sports Medicine 18:588-593.
Smith LL (1991): Acute inflammation: the underlying mechanism in delayed onset muscle soreness? Medicine and Science in Sports and Exercise 23:542-551.
Smith LL, Keating MN, Holbert D, Spratt DJ, McCammon MR, Smith SS and Israel RG (1994): The effects of athletic massage on delayed onset muscle soreness, creatine kinase, and neutrophil count:A preliminary report. Journal of Sports Physical Therapy 19:93-99.
Stauber WT (1996): Delayed-onset muscle soreness and muscle pain. In Zachazewski J, Magee D and Quillen W (Eds): Athletic Injuries and Rehabilitation. Sydney: WB Saunders Company, pp. 92-97.
Tiidus PM (1997): Manual massage and recovery of muscle function following exercise:A literature review. Journal of Sports Physical Therapy 25:107-112.
Tiidus PM and Shoemaker JK (1995): Effleurage massage, muscle blood flow and long-term post-exercise strength recovery. International Journal of Sports Medicine 16:478-483.
Response to Statements of the Speaker for the Negative:
The principle issues presented for the negative included:
a) lack of an inflammatory response to EIMD reflected the inappropriateness of physiotherapy intervention, and
b) the injury is irreversible and therefore prevention is the only intervention indicated.
The role of inflammation in EIMD has been an area of conflict however it is now generally accepted that it plays a part in the overall sequence of events. The cardinal signs of inflammation such as swelling, warmth and pain are present even in the absence of bleeding. Therefore, the physiotherapeutic modalities/techniques described above aimed at reducing the effects of the inflammatory response can reduce the pain perception and enhance muscle performance.
It is true that the tissue disruption following EIMD cannot be reversed however the production of prostaglandins can be affected. If production is decreased prior to a large fluid accumulation by retarding the inflammatory response and reducing fluid compartmental pressure, DOMS should be reduced.
Physiotherapy does have a role in ameliorating the DOMS response to EIMD. The physiotherapists role ranges from preventative to alleviation of symptoms. Knowledge of exercise prescription and time course of injury allows physiotherapists to effectively educate, treat and prescribe appropriate exercises specific to clients needs.
Negative Argument by Beate Lokken
"Unaccustomed exercises may produce a temporary condition of muscle soreness; this soreness will disappear after a few days without any intervention"
Proposed sequence for the development of DOMS
Unaccustomed exercises using eccentric muscle actions (downhill running, slowly lowering weights)
High muscle forces damage sarcolemma causing release of cytosoloc enzymes and myoglobin.
Damage to muscle contractile myofibrils and noncontractile structures.
Metabolites (calcium) accumulate to abnormal levels in the muscle cell. This produces more cell damage and reduced force capacity.
DOMS!!! Resulting from inflammation, tenderness and pain.
The inflammation process begins. The muscle cell heals; the adaptive process is complete, and the muscle is more resistant to damage from subsequent exercise.
Presenting signs & symptoms 24 - 48 hrs post-exercise:
- Performance deficit /weakness
- Muscle damage (Myofiber and connective tissue )
- Muscle soreness and stiffness
- Muscular swelling
- Inflammation !???
Tauma vs. DOMS
- Absence of bleeding
- Pain vs. soreness
-Heat/swelling/pain/loss of function vs. warm swollen muscles/stiffness/weakness
- Exclution of agents and modalities
Treatment of DOMS
No strong evidence of physiotherapy modalities being efficient.
Can stimulate fluid movement however, reduce swelling and soreness if nociceptor activated. And thereby reduce some soreness.
No Drugs - calcium +/-
Hydromassage and warm underwater water-jet massage improves recovery from intense physical exercise.
-through regular exercise
-exercising at short or long muscle lengths???
1. Strenous activity - especially eccentric exercises - causes injury or trauma to the muscle, its musculotendinous junction or both.
2. Injury and/or trauma initiates an inflammatory response resulting in muscles feeling painful and swollen.
3. Pain occurence is delayed approximately 8 hours postactivity and gradually increases, peaking 24 to 48 hours postexercis before gradually subsiding to preexercise levels.
4. Trauma results in significantly increased levels of muscle proteins and other breakdown products of muscle and collagen in the blood and/or urine.
5. Pain is associated with decreased range of motion and strength.
6. Trauma or resulting pain may directly or indirectly result in muscle spasms and a pain-spasm feedback cycle.
Little research exists on the prevention and treatment of DOMS.
Presentation of two studies on modalities treating DOMS:
"Effect of TENS, cold, and a combination treatment on pain, decreased ROM, and strength loss associated with DOMS"
-Compare the changes in preceived, elbow extension range of motion and strength loss in subjects experiencing DOMS in the elbow flexor muscle group following a single treatment with either TENS , cold, a combination of TENS and cold, sham TENS or 20 minutes rest.
-Compare the effects of combining static streching with these treatments.
-Determine if decreased pain is accompanied by restoration of strength.
-Cold, TENS and the combined treatment resulted in significant decreases in perceived
-Treatments with cold resulted in a significant increase in elbow extention range of motion.
-Static streching reduced perceived pain.
- Small changes in muscle strength were observed following treatment or stretching regardless of the treatment group.
Muscle weakness associated with DOMS is not the result of inhibition caused by pain.
Modalities are effective in treating the pain and muscle spasm associated with DOMS, and that decreased pain may not be an accurate indicator of the recovery of muscle strength.
"The effeects of ice massage, ice massage with exercise, and exercise on the prevention and treatment of delayed onset muscles soreness"
22 subjects in 4 groups.
ROM, strength, perceived soreness and serum creatine kinase (CK) levels.
300 consentric/eccentric contractions of the elbow flexors with 90% of their 10 repetition maximum to induce DOMS.
Treatments 0, 2 ,4 ,6, 24, 48, 72 and 96 hours postexercise.
Ice: began treatment too late and did not treat often enough. Can't conclude on effect!
High correlation between perceived soreness at work and rest indicated that the mechanism of pain manifests itself in resting muscles and is not isolated to the contractile process.
Muscle contraction seems to decrease the soreness indicated by reduced CK levels and by having the lowest peak soreness at rest scores.
Total ROM increased as the pain decreased.
Structural changes occured, evidenced by the significant increases in serum CK levels over time.
Strength decreases because of reluctance to use sore muscles and from loss of inherent force-producing capacity within the muscles.
The exercise group has the smallest increases in soreness and CK. i.e. high speed voluntary muscle contraction is effective in decreasing muscle soreness.
The therapeutic use of ice and exercise, combined or used seperately was not effective in reducing the symptoms of DOMS
Patterns in the data suggest that ice application may be contraindicated in the treatment of DOMS. Because the ice with exercise group had greater decrease in ROM and strength and greater increase in soreness and CK than the exercise group.
Chleboun G S, Howell J N, Conatser RR and Giesey JJ (1998): Relationship between muscle swelling and stiffness after eccentric exercise. Medicine and Science in Sport and Exercise 30(4): 529-535.
Clarkson PM and Newman DJ (1995): Associations between muscle soreness, damage and fatigue In Fatigue. Edited by Simon C. Gandevia et al. Plenum Press New York.
Denegar C. R. and Perrin D.H. (1992) Effect of transcutaneous eletrical nerve stimulation, cold and a combination treatment on pain, decreased range of motion, and strength loss associated with delayed onset muscle soreness. Journal of Athletic Training. 27(3): 200-206.
Isabell W K, Durrant E, Myrer W and Anderson S (1992): The effects of ice massage, ice massage wirh exercise, and exercise on the prevention and treatment of delayed onset muscle soreness. Journal of Athletic Training 27(3): 208-217.
Thomasik M (1983): Effect of hydromassage on changes in blood electrolyte and lactic acid levels and haematocrit value after maximal effort. Acta Physiologica Polonica 34(2): 257-261. (Abstract)
Viitasalo JT, Kaappola R, Korjus R, Levola T, Mononen HV, Rusko HK and Takala TES (1995): Warm underwater water-jet massage improves recovery from intense physical exercise. European Journal of Applied Physiology and Occupational Physiology 71(5): 431-438.
- 06-11-2003, 06:42 PM
Does this mean, in a nutshell, something like :
"If you have DOMS out of doing heavy sets of low reps, that is proportional to the amount of damage done to your muscles, and thus possibly indicates how 'good' your workout was *BUT* DOMS from other causes don't mean squat" ???
- 06-11-2003, 07:14 PM
basically I think that was what was being argued here. Personally, I am on a quest to see if I can find a way to relieve some of the symptoms of DOMS for me. It isn't that bad, just annoying at times..
06-28-2003, 10:50 PM
Best cure for Doms I found is this:
Hot tub post workout, followed by visit of asian massage spa. Long massage by 90 pound asian girl, followed by "happy ending"
repeat with another 90 pound asian girl if DOMS continues
06-28-2003, 11:06 PM
06-28-2003, 11:09 PM
Bro, I just recently got a trip to one as a gift. I didnt get the happy ending, but this girl walked up and down my back and cracked each vertebrae with her toes. It was simply amazing, and when she was done with me, you could have poured me into a bucket..lol.
It is an experience well worth trying!!
06-28-2003, 11:13 PM
I will have to check that out.. I have had a deep tissue massage... now that has really been a great experience.. speaking of which I need to schedule one of those soon..
02-09-2008, 03:21 AM
10-01-2008, 03:14 PM
Hey, IMHO DOMS is the 800 pound gorilla in the bodybuilding community. I have gotten pretty strong for a skinny guy by lifting hard, eating right, and allowing my muscles to heal properly between workouts for a given body part.
Building muscle basically involves
1 challenging a muscle group with a workout
2 allowing it to heal; it will adapt to the challenge, growing back stronger than it was in the first place
By spending an hour in the gym, or even half an hour if you spend it wisely, it is possible to do a great job of step 1 for several muscle groups. It is impossible to overemphasize the importance of proper warmup and warmdown to maximize the hypertrophic aspects of step 1 and avoid overtraining and injury (overtraining is itself a form of injury).
Proceeding to step 2, the AM community is rightly fixated on the importance of eating and supplementing strategically to put the body in an anabolic state that will optimize the healing process. A good training regimen, combined with smart eating and supplementing is for most people the cornerstone to a muscle-building program.
I would like to see, however, more of an emphasis on DOMS prevention, strategies for dealing with DOMS, and the importance of rest. Part of the reason for this is my body type: ecto, my mindset: overachiever, and whatever other genetic factors make me a hyper-responder to creatine who is particularly predisposed to DOMS.
One muscle group above all gets very sore when I lift free weights: the hamstrings. I recall vividly the first time I deadlifted. I was reasonably strong for a first-time deadlifter, doing several sets at 135. I was totally unprepared, however, for what happened thereafter: I was sore for literally two weeks after.
For me, lifting involves a great deal of commitment. After a hard day of training, I am pretty much spent the next day, and I have difficulty accomplishing work related tasks that are otherwise easy.
This says several things to me: I need to increase the intensity of my workouts gradually. And as stated before, warmup and warmdown are extremely important.
As for my hamstrings, I think I need to be extra-careful. Years of running have made my legs very strong, but also relatively inflexible. The male hamstring is notorious as perhaps the most inflexible body part, and I believe I am genetically endowed with pretty short hamstrings. This isn't just a matter of muscle, but also tendon and connective tissue. I also have unusually strong calves / glutes / quads, and I believe this somehow increases the tension on my hams.
Anyway, regardless of the reason, I have strong legs and my hams are by far the weak link in my body. I will be thinking about smart ways to get them to catch up.
Does anyone have any suggestions?
01-15-2009, 05:18 AM
01-22-2009, 07:53 PM
Cheung K, Hume P, Maxwell L.
School of Community Health and Sports Studies, Auckland University of Technology, Auckland, New Zealand.
Delayed onset muscle soreness (DOMS) is a familiar experience for the elite or novice athlete. Symptoms can range from muscle tenderness to severe debilitating pain. The mechanisms, treatment strategies, and impact on athletic performance remain uncertain, despite the high incidence of DOMS. DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity. DOMS is also common when athletes are first introduced to certain types of activities regardless of the time of year. Eccentric activities induce micro-injury at a greater frequency and severity than other types of muscle actions. The intensity and duration of exercise are also important factors in DOMS onset. Up to six hypothesised theories have been proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. However, an integration of two or more theories is likely to explain muscle soreness. DOMS can affect athletic performance by causing a reduction in joint range of motion, shock attenuation and peak torque. Alterations in muscle sequencing and recruitment patterns may also occur, causing unaccustomed stress to be placed on muscle ligaments and tendons. These compensatory mechanisms may increase the risk of further injury if a premature return to sport is attempted.A number of treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated dosage-dependent effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used. Cryotherapy, stretching, homeopathy, ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms. Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary. Athletes who must train on a daily basis should be encouraged to reduce the intensity and duration of exercise for 1-2 days following intense DOMS-inducing exercise. Alternatively, exercises targeting less affected body parts should be encouraged in order to allow the most affected muscle groups to recover. Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of, or during, the sporting season in order to reduce the level of physical impairment and/or training disruption. There are still many unanswered questions relating to DOMS, and many potential areas for future research.
Basically cryotherapy has still been unproven. Massage has shown some promise though:
Zainuddin Z, Newton M, Sacco P, Nosaka K.
Edith Cowan University, Joondalup, Western Australia, Australia.
CONTEXT: Delayed-onset muscle soreness (DOMS) describes muscle pain and tenderness that typically develop several hours postexercise and consist of predominantly eccentric muscle actions, especially if the exercise is unfamiliar. Although DOMS is likely a symptom of eccentric-exercise-induced muscle damage, it does not necessarily reflect muscle damage. Some prophylactic or therapeutic modalities may be effective only for alleviating DOMS, whereas others may enhance recovery of muscle function without affecting DOMS. OBJECTIVE: To test the hypothesis that massage applied after eccentric exercise would effectively alleviate DOMS without affecting muscle function. DESIGN: We used an arm-to-arm comparison model with 2 independent variables (control and massage) and 6 dependent variables (maximal isometric and isokinetic voluntary strength, range of motion, upper arm circumference, plasma creatine kinase activity, and muscle soreness). A 2-way repeated-measures analysis of variance and paired t tests were used to examine differences in changes of the dependent variable over time (before, immediately and 30 minutes after exercise, and 1, 2, 3, 4, 7, 10, and 14 days postexercise) between control and massage conditions. SETTING: University laboratory. PATIENTS OR OTHER PARTICIPANTS: Ten healthy subjects (5 men and 5 women) with no history of upper arm injury and no experience in resistance training. INTERVENTION(S): Subjects performed 10 sets of 6 maximal isokinetic (90 degrees x s(-1)) eccentric actions of the elbow flexors with each arm on a dynamometer, separated by 2 weeks. One arm received 10 minutes of massage 3 hours after eccentric exercise; the contralateral arm received no treatment. MAIN OUTCOME MEASURE(S): Maximal voluntary isometric and isokinetic elbow flexor strength, range of motion, upper arm circumference, plasma creatine kinase activity, and muscle soreness. RESULTS: Delayed-onset muscle soreness was significantly less for the massage condition for peak soreness in extending the elbow joint and palpating the brachioradialis muscle (P < .05). Soreness while flexing the elbow joint (P = .07) and palpating the brachialis muscle (P = .06) was also less with massage. Massage treatment had significant effects on plasma creatine kinase activity, with a significantly lower peak value at 4 days postexercise (P < .05), and upper arm circumference, with a significantly smaller increase than the control at 3 and 4 days postexercise (P < .05). However, no significant effects of massage on recovery of muscle strength and ROM were evident. CONCLUSIONS: Massage was effective in alleviating DOMS by approximately 30% and reducing swelling, but it had no effects on muscle function.
Basically whoever figures out how to "cure" DOMs will be a very rich and very respected person in exercise physiology and research.
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